MECONIUM ASPIRATION SYNDROME: You should get it right.

Meconium aspiration syndrome refers to breathing problems that a baby may have when no other, attributable cause exists after the baby has passed meconium into the amniotic fluid during labour or delivery. It usually occurs if the baby breathes in (aspirates) this fluid into the lungs.

Meconium is the first intestinal discharge from the baby after delivery – a viscous, dark-green substance composed of intestinal epithelial cells, lanugo, mucus, and intestinal secretions like bile. At 85-95%, water is the prominent liquid constituent of meconium; intestinal secretions, mucosa cells and elements of swallowed amniotic fluid like lipids and proteins comprise the other 5-15%.

meconium aspiration syndrome

Meconium is sterile (it doesn’t contain bacteria) – distinguishing it from the normal stool. When babies are distressed inside the uterus (womb), they can pass meconium into the amniotic fluid.

Inside the uterus, any form of foetal hypoxia stimulates the maturing gastrointestinal tract (digestive system) to pass out meconium. The Vagus nerve facilitates the stimulation due to a head or spinal cord compression. Because the gastrointestinal tract matures as the foetus approaches term, vagal stimulation may initiate peristalsis; the rectal sphincter relaxes and eventually, the baby passes meconium.

Through altering it, meconium reduces the antibacterial activity of the amniotic fluid. It increases the risk of perinatal bacterial infection. Meconium irritates the foetal skin – increasing the incidence of erythema toxicum.

This aspiration induces hypoxia via four pulmonary effects: airway obstruction, surfactant dysfunction, chemical pneumonitis, and pulmonary hypertension.

Meconium may completely obstruct the airways which culminate in atelectasis. The partial obstruction causes air trapping and hyperdistention of the alveoli: we term this, the ball-valve effect. Hyperdistention of the alveoli occurs from airway expansion during inhalation and airway collapse around inspissated meconium in the airway, causing increased resistance during exhalation. The gas that is trapped can cause a pneumothorax, pneumomediastinum, or pneumopericardium.

Meconium deactivates surfactant and may also inhibit surfactant synthesis. Several constituents of meconium, especially the free fatty acids (palmitic, stearic, oleic acids), have a higher, minimal surface tension than surfactant and strip it from the alveolar surface, that results in diffuse atelectasis (lung collapse).

Enzymes, bile salts, and free fatty acids in meconium irritate the airways and parenchyma. The baby’s body releases cytokines such as tumour necrosis factor (TNF-α) and interleukin (IL)-1β, IL-6, IL-8, IL-13, which initiate a diffuse pneumonitis that may begin within a few hours of aspiration. The result is the gross ventilation-perfusion (V/Q) mismatch.

To complicate matters further, many infants with meconium aspiration syndrome have primary or secondary persistent pulmonary hypertension as a result of chronic in utero stress and thickening of the pulmonary vessels. It further contributes to the hypoxaemia caused by meconium aspiration syndrome.

Various factors promote the passage of meconium in utero: Placental insufficiency, maternal hypertension, preeclampsia, oligohydramnios, maternal drug abuse (tobacco and cocaine), maternal infection (chorioamnionitis), and foetal hypoxia.

For meconium aspiration syndrome to develop, meconium must be present in the amniotic fluid. However, not all neonates whose liquor is stained with meconium develop this condition. Nonetheless, to diagnose meconium aspiration syndrome, meconium must be present in the amniotic fluid, if not, the neonate must exhibit signs and symptoms of respiratory distress with characteristic abnormalities on the x-ray.

Signs and symptoms of respiratory distress include cyanosis, grunting, nasal flaring, chest wall indrawing, tachypnoea, barrel chest, and rales and rhonchi on auscultation.

You may observe yellow-green staining of fingernails, umbilical cord, and skin. Because meconium pigments can be absorbed in the lungs and eventually excreted in the urine, you may note green urine among these neonates within 24 hours after birth.

Investigations are paramount for both the diagnosis and appropriate management. Ideally, we measure the arterial blood gases – pH, carbon dioxide partial pressure (pCO2), and oxygen partial pressure (pO2). We also continuously monitor the neonate’s oxygenation by pulse oximetry. By doing this, we keep the neonate’s acid-base status in check.

Because perinatal stress commonly leads to a syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and acute kidney injury, we obtain the neonate’s sodium, potassium, and calcium concentrations at 24 hours after birth.

We also obtain blood for a complete blood count. Here, we are interested in the white cell count, especially the neutrophil count, haemoglobin level, and platelet count. When there’s perinatal blood loss or an infection, the new-born baby stands a high risk of perinatal stress.

Haemoglobin and haematocrit levels must be sufficient to guarantee adequate oxygen-carrying capacity. Abnormally high red blood cell count (polycythaemia) may signal chronic foetal hypoxia: this is usually associated with decreased pulmonary blood flow and may worsen the hypoxia associated with meconium aspiration syndrome. Low platelets increase the risk of haemorrhage. A small or high neutrophil count may imply a perinatal, bacterial infection. And if so, a blood culture may be warranted – little evidence exists to ascertain the benefits of empiric antibiotic therapy after the clinicians obtain blood culture in the absence of maternal fever or prolonged rupture of membranes.

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We do chest radiography to confirm the diagnosis and assess the extent of lung damage, identify areas of lung collapse and air leakages, and to ensure that we’ve correctly positioned the endotracheal tube and umbilical catheters.

We request for echocardiography to assess the cardiac function and the severity of pulmonary hypertension and right-to-left shunting. Normal cardiac function is paramount to ensure sustained oxygen delivery to all tissues.

Treatment of meconium aspiration syndrome involves both medical and surgical endeavours.
We keep the baby dry and maintain optimal body temperature; place the baby on oxygen to help deliver oxygen to the circulation; we may need a surfactant to enhance the lungs functioning; we may add antibiotics if there’s evidence of an infection. To decrease pulmonary resistance and increase lung blood flow, we may give respiratory gases like nitric oxide. Typically, a neonatologist inserts drainage tubes in the chest to manage air leak syndromes. We can also consult the paediatric surgeon in cases where fibrin glue is necessary.

Visit UpToDate, Medscape, Merck Manuals, or NEJM for more information about this topic

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